Acute kidney injury Flashcards

1
Q

What is AKI?

A

Acute kidney injury (AKI) is an acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output.

= Electrolyte imbalance, fluid retention, uraemia, and azotaemia (high levels of nitrogen -containing compounds (such as urea, creatinine, various body waste compound)

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2
Q

what are the RF for AKI?

A

HTN
CKD
Nephrotoxic drugs - NSAIDs/ACEi/ARB/aminoglycosides
Sepsis
Diabetes

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3
Q

What are the causes underling AKI?

A

Causes of Acute kidney injury is categorised into:

Pre-renal : Hypoperfusion or low effective circulating volume
Intra-renal: Destruction to renal structure
Post-renal: Obructive neuropathy

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4
Q

What are the underlying causes of pre-renal AKI

A

Pre-renal AKI~ Reduced Glomerular Perfusion - 80%

Low effective circulating volume (Hypovolemia)
* Dehydration
* Bleeding
* Shock
* D/V

Glomerular Hypoperfusion
* Cirrhosis
* Congestive Heart failure
* Renal artery stenosis

DRUGS - ANT-HTN meds

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5
Q

Describe the pathophysiology of pre-renal AKI

A

Reduced blood volume = reduced renal perfusion
This causes a reduction in GFR = less creatinine excreted

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6
Q

What are the underlying causes of Intra-Renal AKI

A

Damage to the kidney further divided by location: Vascular, Glomerular, Tubular, Interstitial

Vascular : Vasculitis, MAHA (macroangiopathic haemolytic anaemia)

Glomerular Nephritis GN- Barrier damage = protein leakage

Acute tubular necrosis ~ prolonged ischaemia, infections, myeloma, nephrotoxins

Acute interstitial nephritis ~ infections, ischaemia, Connective tissue disorder

Infection=inflamm=scarring
reduce perfusion=necrosis
tissue damage = leakage

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7
Q

What are the underlying causes of post-Renal AKI

A

Post-renal AKI ~ Obstruction to the urinary tract from:

Renal stones
BPH - Enlarged prostate
Genitourinary tumours
Infection - Pyelon nephritis

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8
Q

How can obstruction to the urinary tract cause post-renal AKI?

A

Obstruction = increase pressure within urinary tract = This backs into renal increasing pa within nephrons = this reduce rate of GFR and also increases fluid build up

May show signs of fluid overload: pulmonary or peripheral oedema and raised JVP

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9
Q

How may AKI present

A
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10
Q

Investigating AKI

A

First : Detection w/ RIFLE CRITERIA
One of:
- Rise in creatinine >26umol/l in 48hrs
- Rise in creatinine >50% baseline within 7 days
- Urine output Less than 0.5ml/kg/h for >6hrs consecutively

Second Calculate severity w/KDIGO system
Uses : Serum creatinine and Urine production

Primary investigations:

Blood Urea : Creatinine ratio
>100:1 - Pre-renal
<40:1 - renal
40-100:1 - Post renal

U/E K+,ca2+,phosphate, h+
FBC - CRP? ~ Infection
VBG - Metabolic acidosis
CXR - Pulmonary odema
Urine dipsticks MC/S- UTI

Imaging:
Renal US - obstruction or hydronephresis
NCCT KUB / XR KUB
Renal biopsy for intra-hepatic

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11
Q

Treating AKI

A

Treat cause
Stop nephrotoxic drugs
Hypovolemia: IV fluid resus saline (0.9% sodium chloride)
Sepsis/pyelonephritis - Starts Ab
Remove obstruction - Bladder Catheter /Nephrostomy

Treat comorbidities:
Fluid overload - oedematous - Loop diuretic Furosemide
Hyperkalaemia (Calcium gluconate)
Metabolic acidosis- Bicarbonate

If AFUK (ACIDOSIS, FLUID OVERLOAD, URAEMIA, K+>6.5 w/ ECG)
——> Dialysis - peritoneal dialysis, haemodialysis

ESRF - Transplant

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12
Q

what the difference between AKI and CKD

A

AKI - Short sx onset, no anemia, no ultrasound change

CKD - >3months, anemia, w/ change on Kidney US

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